Morphine stimulates mu opioid receptors to provide the desired effect of analgesia, but in doing so can also precipitate many undesired effects. This patient has multiple signs of opioid toxicity, including miosis (ie, pinpoint pupils), respiratory depression (evidenced by slow respiratory rate and respiratory acidosis), and CNS depression (eg, somnolence, coma). Morphine is primarily metabolized by the liver via glucuronidation to form 2 major metabolites. These metabolites, morphine-3-glucoronide and morphine-6-glucoronide, then undergo renal elimination via excretion in the urine. Because the metabolites are metabolically active, renal dysfunction can lead to metabolite accumulation and opioid toxicity. Morphine-6-glucoronide is particularly responsible for toxicity, acting as a more potent mu opioid receptor agonist than morphine itself.
Due to its metabolically active and renally cleared metabolites, morphine requires careful monitoring when used in patients with renal dysfunction. When opioid pain control is needed in such patients, fentanyl or hydromorphone is often preferred as these drugs are predominantly hepatically cleared.
Also, morphine-6-glucuronide is excreted renally. So, morphine would cause toxicity in patients with reduced renal functions.